Abstract

The efficiency of pulmonary gas exchange has long been assessed using the alveolar-arterial difference in PO2, the A-aDO2, a construct developed by Richard Riley ~70years ago. However, this measurement is invasive (requiring an arterial blood sample), time consuming, expensive, uncomfortable for the patients, and as such not ideal for serial measurements. Recent advances in the technology now provide for portable and rapidly responding measurement of the PO2 and PCO2 in expired gas, which combined with the well-established measurement of arterial oxygen saturation via pulse oximetry (SpO2) make practical a non-invasive surrogate measurement of the A-aDO2, the oxygen deficit. The oxygen deficit is the difference between the end-tidal PO2 and the calculated arterial PO2 derived from the SpO2 and taking into account the PCO2, also measured from end-tidal gas. The oxygen deficit shares the underlying basis of the measurement of gas exchange efficiency that the A-aDO2 uses, and thus the two measurements are well-correlated (r2~0.72). Studies have shown that the new approach is sensitive and can detect the age-related decline in gas exchange efficiency associated with healthy aging. In patients with lung disease the oxygen deficit is greatly elevated compared to normal subjects. The portable and non-invasive nature of the approach suggests potential uses in first responders, in military applications, and in underserved areas. Further, the completely non-invasive and rapid nature of the measurement makes it ideally suited to serial measurements of acutely ill patients including those with COVID-19, allowing patients to be closely monitored if required.

Highlights

  • For the lung to exchange gas (O2 from the inspired air into the blood, and CO2 from the blood to the expired gas), alveolar gas and pulmonary capillary blood must be brought into close apposition across the thin alveolar-capillary membrane

  • The study showed that the oxygen deficit (OD) was sensitive to the mild gas exchange impairment associated with healthy aging, even while breathing air, but that individual errors at high values of SpO2 meant that the measurement was not likely to be useful in individual subjects at SpO2 values above 94%

  • This study showed that the non-invasive approach provided a convenient, low cost, and accurate alternative to the use of an arterial blood gas (ABG) to measure the magnitude of the gas exchange disruption in patients with pulmonary disease

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Summary

INTRODUCTION

For the lung to exchange gas (O2 from the inspired air into the blood, and CO2 from the blood to the expired gas), alveolar gas and pulmonary capillary blood must be brought into close apposition across the thin alveolar-capillary membrane. While a Hill-n of 2.7 provides an excellent fit to the experimentally determined values of saturation and PO2 over the entire range of saturation (Severinghaus, 1966; Prisk and West, 2019), in practice, only blood oxygen saturations in the range of 75–100% are likely to be encountered in patients. Because the end-tidal gas partial pressure reflects the alveolar PCO2, the leftward or rightward shift of the O2-Hb dissociation curve from a PCO2 different to the normal value of 40 mmHg (the Bohr effect) can be accounted for. Assuming otherwise normal conditions for temperature, base excess and 2,3-dpg is determined (Prisk and West, 2019) This is used to correct for changes in alveolar PCO2, assuming this is equal to arterial PCO2, an equivalence that has been long established (Comroe and Dripps, 1944). This should not be confused with the “oxygen deficit” that provides a measure of the anaerobic contribution during exercise (Krogh and Lindhard, 1920; Medbo et al, 1988)

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